Fig. 5. Bone cell defects in the absence of EGFR. Histological sections through the tibiae of control (A), hEGFR^KI/KI (B) and Egfr^-/- mice (C) at postnatal day 1. The black bar marks the zone of hypertrophic chondrocytes, which is markedly increased in both hEGFR^KI/KI and Egfr^-/- long bones. (D) X-galactosidase (X-gal) staining of an E14.5 Egfr^+/- foetus showing EGFR expression (blue stain) in the ossification center of the vertebrae. Inset shows a higher magnification of the region boxed in D with arrows indicating X-gal staining in chondroblasts. (A-C) Haematoxylin and Eosin staining; (D) X-gal and Eosin staining. (E) The proliferation of chondrocytes was measured by Ki67 staining on bone sections of mice of the indicated genotypes. The data represent the mean±s.d. of the number of Ki67-positive chondrocytes present on six different sections. (F,G) Cumulative cell number of hEGFR^KI/KI (F) and Egfr^-/- (G) primary osteoblasts isolated from newborn calvariae showing reduced proliferation of hEGFR^KI/KI and Egfr^-/- osteoblasts at the end of the culture period. (H,I) Primary osteoblasts derived from hEGFR^KI/KI (H) and Egfr^-/- (I) neonatal calvariae showed enhanced bone nodule formation compared with controls. Data represent the mean±s.e.m. (J) Western blot analysis showing EGFR (180 kDa) protein expression in hEGFR^KI/KI and control osteoblasts. Anti-Actin immunoblotting was used as an internal protein loading control.

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